Previously, we identified PRMT6 as a key regulator of liver fibrosis development in mice fed high-fat diet, alcohol, or treated with thioacetamide as well as mice on a chow diet at 1 year of age.18 One of the main protective functions of PRMT6 is macrophage integrin methylation, which reduces their profibrotic function in liver disease induced by multiple factors: high-fat diet, alcohol, thioacetamide treatment, or aging.23 In this study, we found that female sex hormone signaling and specifically, estrogen, suppresses integrin gene expression. This evidence concerns the gene PRMT6 and Hepatic fibrosis.